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Ultraviolet light
About: Ultraviolet light is a research topic. Over the lifetime, 49494 publications have been published within this topic receiving 843151 citations.
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TL;DR: It is shown that vertical base stacking, and not base pairing, determines the fate of excited singlet electronic states in single- and double-stranded oligonucleotides composed of adenine (A) and thymine (T) bases.
Abstract: Solar ultraviolet light creates excited electronic states in DNA that can decay to mutagenic photoproducts. This vulnerability is compensated for in all organisms by enzymatic repair of photodamaged DNA. As repair is energetically costly, DNA is intrinsically photostable. Single bases eliminate electronic energy non-radiatively on a subpicosecond timescale1, but base stacking and base pairing mediate the decay of excess electronic energy in the double helix in poorly understood ways. In the past, considerable attention has been paid to excited base pairs2. Recent reports have suggested that light-triggered motion of a proton in one of the hydrogen bonds of an isolated base pair initiates non-radiative decay to the electronic ground state3,4. Here we show that vertical base stacking, and not base pairing, determines the fate of excited singlet electronic states in single- and double-stranded oligonucleotides composed of adenine (A) and thymine (T) bases. Intrastrand excimer states with lifetimes of 50–150 ps are formed in high yields whenever A is stacked with itself or with T. Excimers limit excitation energy to one strand at a time in the B-form double helix, enabling repair using the undamaged strand as a template.
414 citations
TL;DR: Here it is demonstrated a process by which the transparent insulating oxide 12CaO·7Al2O3 (refs 7–13) can be converted into an electrical conductor and suggested that this concept can be applied to other main-group metal oxides, for the direct optical writing of conducting wires in insulating transparent media and the formation of a high-density optical memory.
Abstract: Materials that are good electrical conductors are not in general optically transparent, yet a combination of high conductivity and transparency is desirable for many emerging opto-electronic applications1,2,3,4,5,6. To this end, various transparent oxides composed of transition or post-transition metals (such as indium tin oxide) are rendered electrically conducting by ion doping1,2,3,4,5,6. But such an approach does not work for the abundant transparent oxides of the main-group metals. Here we demonstrate a process by which the transparent insulating oxide 12CaO·7Al2O3 (refs 7–13) can be converted into an electrical conductor. H- ions are incorporated into the subnanometre-sized cages of the oxide by a thermal treatment in a hydrogen atmosphere; subsequent irradiation of the material with ultraviolet light results in a conductive state that persists after irradiation ceases. The photo-activated material exhibits moderate electrical conductivity (∼0.3 S cm-1) at room temperature, with visible light absorption losses of only one per cent for 200-nm-thick films. We suggest that this concept can be applied to other main-group metal oxides, for the direct optical writing of conducting wires in insulating transparent media and the formation of a high-density optical memory.
413 citations
TL;DR: It is shown that the high-mobility group box 1 protein (HMGB1) is a redox-sensitive regulator of the balance between autophagy and apoptosis, representing a suitable target when coupled with conventional tumor treatments.
Abstract: The functional relationship and cross-regulation between autophagy and apoptosis is complex. In this study we show that the high-mobility group box 1 protein (HMGB1) is a redox-sensitive regulator of the balance between autophagy and apoptosis. In cancer cells, anticancer agents enhanced autophagy and apoptosis, as well as HMGB1 release. HMGB1 release may be a prosurvival signal for residual cells after various cytotoxic cancer treatments. Diminished HMGB1 by short hairpin RNA transfection or inhibition of HMGB1 release by ethyl pyruvate or other small molecules led predominantly to apoptosis and decreased autophagy in stressed cancer cells. In this setting, reducible HMGB1 binds to the receptor for advanced glycation end products (RAGEs), but not to Toll-like receptor 4, induces Beclin1-dependent autophagy and promotes tumor resistance to alkylators (melphalan), tubulin disrupting agents (paclitaxel), DNA crosslinkers (ultraviolet light) and DNA intercalators (oxaliplatin or adriamycin). On the contrary, oxidized HMGB1 increases the cytotoxicity of these agents and induces apoptosis mediated by the caspase-9/-3 intrinsic pathway. HMGB1 release, as well as its redox state, thus links autophagy and apoptosis, representing a suitable target when coupled with conventional tumor treatments.
413 citations
TL;DR: These results identify retroviral proteins that interact with a mammalian toll receptor and show that direct activation by such viruses may initiate in vivo infection pathways.
Abstract: Although most retroviruses require activated cells as their targets for infection, it is not known how this is achieved in vivo. A candidate protein for the activation of B cells by either mouse mammary tumor virus (MMTV) or murine leukemia virus is the toll-like receptor 4 (TLR4), a component of the innate immune system. MMTV caused B cell activation in C3H/HeN mice but not in C3H/HeJ or BALB/c (C.C3H Tlr4lps-d) congenic mice, both of which have a mutant TLR4 gene. This activation was independent of viral gene expression, because it occurred after treatment of MMTV with ultraviolet light or 2,2′-dithiodipyridine and in azidothymidine-treated mice. Nuclear extracts prepared from the lymphocytes of MMTV-injected C3H/HeN but not C3H/HeJ mice showed increased nuclear factor κB activity. Additionally, the MMTV- and Moloney murine leukemia virus envelope proteins coimmunoprecipitated with TLR4 when expressed in 293T cells. The MMTV receptor failed to coimmunoprecipitate with TLR4, suggesting that MMTV/TLR4 interaction is independent of virus attachment and fusion. These results identify retroviral proteins that interact with a mammalian toll receptor and show that direct activation by such viruses may initiate in vivo infection pathways.
411 citations
TL;DR: The action spectrum of the photoinhibition of dye reduction by chloroplasts and lyophylized Anacystis cells indicated that the damage caused by visible light is due to quanta absorbed by photosystem II, however, since system I might not be involved in dye reduction, the spectra may reflect only damage to Photosystem II.
Abstract: A study was made of photoinhibition of spinach chloroplast reactions. The kinetics and spectral characteristics of the photoinhibition over a range between 230 and 700 mmu have been examined. The decline of activity due to preillumination was independent of wavelength, and dependent upon the number of quanta applied, not upon the rate of application. The effectiveness spectra of photoinhibition indicate that active ultraviolet light is absorbed by a pigment which is not a normal light absorber for photosynthesis and acts with a high quantum efficiency (> 0.1) for photoinhibition.Active visible light is absorbed by the pigments which sensitize photosynthesis (chlorophyll, carotenoids). A very low quantum efficiency (about 10(-4)) was observed for the photoinhibition with visible light.The action spectrum of the photoinhibition of dye reduction by chloroplasts and lyophylized Anacystis cells indicated that the damage caused by visible light is due to quanta absorbed by photosystem II. However, since system I might not be involved in dye reduction, the spectra may reflect only damage to photosystem II.
410 citations